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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The case of a 50 year old male with the Fiessinger-Leroy-Reiter syndrome, ankylosing spondylitis and generalised pustular psoriasis is reported. This condition wax complicated by non-obstructive cardiomyopathy, congestive cardiac failure and first-degree atrioventricular block, the site of which was localised by electrophysiological studies (nodal block with an infrahisian conduction defect). After failure of several therapeutic regimes, a spectacular improvement was obtained with Methotrexate associated with a diuretic; the signs of heart failure regressed and the cardiomyopathy stablised. A parallel improvement was seen in the skin, cardiac and articular lesions and has been maintained with an 18 months follow-up. Left ventricular performance was studied by echocardiography. The mechanism of the beneficial effect of Methotrexate is unclear; this therapeutic trial is to be extended to include other cases of primary cardiomyopathy without obstruction.
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PMID:[Fiessinger-Leroy-Reiter syndrome with non-obstructive cardiomyopathy treated with methotrexate]. 11 79

The ultrastructure of the atrio-ventricular junction in the rat heart fixed in situ was studied on serial fine sections. The relationships between the specialized tissue and the nervous system were studied after labelling adrenergic endings with 5-OH-dopamine. Among the various types of nerve endings a distinction may be made between: 1) adrenergic or cholinergic free endings; 2) large "cluster" endings of the cholinergic types, seen mainly in the equatorial regions of nodal cells; 3) small diameter cholinergic before the development of heart failure or significant card synaptic images; 4) afferent neurons, whose endings, rich in glycogen and mitochondria supply the conduction tissue fibres, getting into or through the muscle fibre. The intermembrane space is then 20 nm. The analogy between the images observed and the ultrastructural aspects of intrafusorial fibres in skeletal muscle is discussed.
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PMID:[Contribution of ultrastructural analysis to the knowledge of the neuromuscular relationships in the nodal and conduction tissue]. 12 Jan 45

Left ventricular pressure and volume during diastole reflect the interaction of ventricular elastic, viscous, and inertial properties, and the completeness of myocardial relazation. Myocardial relaxation may be impaired in the acutely ischemic ventricle, partly accounting for the abnormal diastolic pressure-volume relation in this condition. Altered elasticity of its wall can cause increased stiffness of the ventricular chamber, as in aortic stenosis, coronary heart disease, and infiltrative cardiomyopathies. In aortic stenosis, increased left ventricular stiffness results in an increase in pressure increment associated with left atrial contraction. Generation of such a high filling pressure is critical in maintaining adequate end diastolic sarcomere stretch in the left ventricle and probably accounts for the frequent deterioration of patients with aortic stenosis after development of atrial fibrillation or nodal rhythm. Many signs and symptoms of cardiac failure, previously attributed to impaired systolic performance, may be due to partly to altered diastolic properties of the ventricular chambers.
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PMID:Diastolic properties of the left ventricle. 76 26

In 1164 cases clinical and electrocardiographical findings were correlated with serum digoxin concentrations (SDC). The diagnosis of digitalis intoxication was based on rhythm disturbances which disappeared on withdrawel of the drug. The mean SDC for patients with digitalis-induced arrhythmias was 3.07 ng/ml compared to 1.02 ng/ml for patients with normal Ecg's and 1.01 ng/ml for patients with rhythm disturbances of other origin. Taking 2.0 ng/ml as the lower limit of digitalis intoxication a more than 85% coincidence was found between the diagnosis based on serial Ecg's and on SDC levels. No signs of cardiac toxicity were found in patients with SDC's less than 1.6 ng/ml, some patients, however, showed normal Ecg's despite SDC's up to 4.5 ng/ml. Patients with SDC's greater than 1.9 ng/ml and normal Ecg's were significantly younger than patients with digitalis-induced arrhythmias at comparable SDC's. Although no definite diagnosis of cardiac toxicity could be established in 327 cases, the clinical data of patients with SDC's of 2.0 ng/ml and greater resemble closely those with digitalis-induced arrhythmias while patients with SDC's less than 2.0 ng/ml showed close resemblance to patients with no cardiac evidence of toxicity with regard to: mean age, kidney function, mean digoxin dosage and mean body weight. Patients with elevated SDC's showed a 45% incidence of severely impaired kidney function in contrast to 28% of the patients with SDC's less than 2.0 ng/ml. Even in patients with normal kidney function the correlation between the orally administered digoxin dosage and SDC levels was poor. The correlation was significantly better when dogoxin was administered intravenously. Therefore knowing the amount of digoxin taken (according to the patient's statement) seems of little benefit in the evaluation of digitalis toxicity. In patients with digitalis-induced arrhythmias mean age and mean body weight were significantly lower, mean creatinine concentration and the incidence of severe cardiac insufficency and of typical ST-T-changes were significantly higher. There was no significant difference in mean potassium concentration and incidence of coronary artery disease compared to nontoxic patients. Compared to patients with cardiac arrhythmias of other origin there were no significant differences in mean age, mean potassium and creatinine concentrations and cardiac insufficiency while the incidence of coronary artery disease was significantly higher among patients with rhythm disturbances of other origin. Every type of rhythm disturbance can be digitalis-induced. Among our patients the incidence of digitalis-induced second-degree atrioventricular block (Wenckebach), ventricular bigeminy, nonparoxysmal nodal tachycardia and PAT with block was significantly higher while patients with rhythm disturbances of other origin showed an equally high incidence of PVB's and prolongation of PQ interval...
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PMID:[Digitalis intoxication: specifity and significance of cardiac and extracardiac symptoms. part I: Patients with digitalis-induced arrhythmias (author's transl)]. 85 52

Adenosine has recently become widely available for the treatment of paroxysmal supraventricular tachycardia. In order to evaluate its role in the management of arrhythmias, we have reviewed the literature on the cellular mechanisms, metabolism, potential for adverse effects, and clinical experience of the efficacy and safety of intravenous adenosine. Adenosine produces transient atrioventricular nodal block when injected as an intravenous bolus. This is of therapeutic value in the conversion to sinus rhythm of the majority of paroxysmal supraventricular tachycardias, which involve the atrioventricular node in a re-entrant circuit. The mean success rate was 93% from over 600 reported episodes. Compared with other antiarrhythmic agents, adenosine is remarkable for its rapid metabolism and brevity of action, with a half-life of a few seconds. It commonly produces subjective symptoms, particularly chest discomfort, dyspnea, and flushing, which are of short duration only. No serious adverse effect has been reported. Arrhythmias may recur within minutes in a minority of patients. Comparative studies have shown that adenosine is as effective as verapamil in the treatment of supraventricular tachycardia, and has less potential for adverse effects. Patients with supraventricular tachycardia should initially be treated using vagotonic physical maneuvers. Immediate electrical cardioversion is indicated if the arrhythmia is associated with hemodynamic collapse. Adenosine is the preferred drug in those patients in whom verapamil has failed or may cause adverse effects, such as those with heart failure or wide-complex tachycardia. The safety profile of adenosine suggests that it should be the drug of first choice for the treatment of supraventricular tachycardia, but only limited comparative data to support this view are available at present.
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PMID:Adenosine and the treatment of supraventricular tachycardia. 160 47

The purpose of this study was to define the prognostic value concerning in-hospital, two-month, and one-year mortality of an early echocardiographic estimation of left ventricular ejection fraction, relative to traditional clinical variables and a clinical prognostic index, in an unselected series of 193 patients following acute myocardial infarction. Left ventricular ejection fraction was determined within 72 hours by echocardiographic wall motion analysis within the frame of a nine-segment model. Clinical variables (age, number of acute myocardial infarctions, reinfarction, heart failure, cardiac arrest, ventricular arrhythmias, asystole, supraventricular tachycardia, nodal rhythm) and a calculated, previously published index, based on these variables, were recorded on day five post infarction and predischarge. The Killip class was recorded at the time of echocardiography. All variables were compared by a multivariate approach (Cox regression model). The results showed that left ventricular ejection fraction was the strongest predictor of early and late mortality and increasingly so over the period of observation. Age and maximal Killip class had a modest additional prognostic value, whereas the composite clinical prognostic index had no predictive power when early left ventricular ejection fraction was included in the statistical model.
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PMID:Prognostication in acute myocardial infarction by early echocardiographic estimation of left ventricular ejection fraction. Multivariate statistical comparison with a clinical prognostic index and its components. 161 23

Fifteen cases of chronic heart block were studied. Eight of them could be designated as idiopathic or primary heart block; the others were associated with hypertension, diabetes and ischaemic heart disease, either singly or in various combinations. In six cases, the whole heart was available for histopathological study of the conduction system. In the other 9 cases, only a portion of the heart muscle was available for examination. A V nodal fibrosis extending upto the proximal bundle of His was seen in all the six whole heart autopsy materials. Fibrosis of the adjacent myocardium was seen in five cases. In three cases, conducting system fibrosis was associated with atherosclerotic (1 case) or diabetic changes (3 cases) of the intramural vessels. In the 9 partial autopsy studies, myocardial fibrosis was seen in two cases, diabetic microangiopathy in one and atherosclerotic changes in two including an old thrombus in one. Thus, diabetic microangiopathy was seen in total four cases. These changes may be responsible for the cardiomegaly and cardiac failure associated with conduction defects observed in diabetes. In the idiopathic group also, heart block could be considered as a significant facet of a primary myocardial degenerative process.
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PMID:Cardiac changes implicated in chronic heart block. 181 5

For the purpose of searching for the underlying mechanism of sudden death, 46 cases of non-traumatic sudden death were selected from autopsied cases during the past 8 years from 1980 to 1987 in the department of legal medicine, St. Marianna university school of medicine. These included 40 males and 6 females ranging from 30 to 60 years of age. Autopsy revealed the existence of cardiac abnormalities in 41 cases (89.1%). Among them, acute myocardial infarction was found in 23 cases (56.1%) and there were 16 cases (39.0%) diagnosed as acute cardiac failure because of the absence of organic abnormality in the heart. Out of the latter cases having undefined etiology of sudden death, 10 cases were selected and histopathological study on the cardiac conduction system was performed by Lev's method. Fatty infiltration in the sinus node, in the atrio-ventricular node and bundle of His was observed in 5 cases, severe stenosis of atrio-ventricular nodal artery in 2 cases and subendocardial hemorrhage of left bundle branch in 1 case. In the remaining case, no pathological abnormality was observed. These results suggest that the organic lesion of the cardiac conduction system could underlies the clinically undefined cause of sudden death.
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PMID:[A histopathological study on the cardiac conduction system in sudden death of unknown origin]. 226 5

Adenosine receptor stimulation, such as by adenosine monophosphate (AMP), elicits systemic vasodilation that may be useful to control cardiac afterload during treatment of acute low-output cardiac failure. This study compared the hemodynamic effects of graded doses of sodium nitroprusside (SNP) with those of AMP when infused alone or in combination with the positive inotropic agent dopamine (DA) in anesthetized dogs. Both SNP (2-25 micrograms.kg-1.min-1) and AMP (200-2500 micrograms.kg-1.min-1) were effective vasodilators and reduced systemic vascular resistance and arterial pressure in a dose-dependent manner. Heart rate and cardiac index were increased by both agents. When compared at dosages that caused similar decreases in arterial pressure, cardiac index was increased more by AMP than by SNP. Also, AMP-induced vasodilation was associated with less tachyphylaxis. Sodium nitroprusside and AMP, at the dosages used, did not depress atrioventricular nodal conduction or antagonize DA-induced increases in renal blood flow. At equivalent decreases in mean arterial pressure, the increase from baseline in cardiac and stroke indices observed with AMP alone was further increased by the concomitant administration of DA. These results suggest that AMP and DA-AMP may offer significant advantages over SNP or DA-SNP in situations where elevation of cardiac output and reduction in afterload are required.
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PMID:Comparison of hemodynamic changes induced by adenosine monophosphate and sodium nitroprusside alone and during dopamine infusion in the anesthetized dog. 229 5

MCI-154 is a potent nonglycoside and non-sympathomimetic cardiotonic agent with a pyridazinone structure. We assessed its cardiac and coronary vasodilator effects by use of isolated, blood-perfused papillary muscle, sinoatrial (SA) node, and atrioventricular (AV) node preparations of dogs. The drug (1-100 nmol) was injected intraarterially. MCI-154 increased the force of contraction of paced and unpaced papillary muscles but failed to affect the rate of automaticity of the latter. It increased sinus rate and shortened AV conduction time by accelerating AV nodal conduction, but in all doses examined it produced no arrhythmias. In all preparations, it increased blood flow. All the effects were long-lasting (1-2 h). MCI-154, however, was not homogeneously effective on these cardiovascular variables. The drug was nearly equieffective in producing a positive inotropic effect and coronary vasodilatation, but less effective in producing positive chronotropic and dromotropic effects. In having such a cardiovascular profile, MCI-154 most resembles milrinone among new cardiotonic agents, although unlike milrinone, its main mechanism of cardiotonic action is believed to be the sensitization of the contractile proteins to Ca2+. Whatever mechanisms are involved, the revealed cardiovascular profile of MCI-154 justifies its clinical trial in the treatment of heart failure.
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PMID:Cardiac and coronary vasodilator effects of the novel cardiotonic agent, MCI-154, assessed in isolated, blood-perfused dog heart preparations. 245 Feb 40


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